Search

Objective:Previous studies of sociodemographic and lifestyle correlates of dietary patterns among young adults have primarily focused on physical activity and smoking, with inconclusive results. This study aims to examine the associations between a broader range of lifestyles of young adults and their patterns of food consumption.Design:Cross-sectional.Setting:Brisbane, Australia.Participants:The data set are from a long running birth cohort study which commenced in 1981. Details of dietary intake and sociodemographic and lifestyle factors were from the 21-year follow-up of the Mater-University of Queensland Study of Pregnancy (MUSP) birth cohort. The effective cohort (n 2665, 57 % women) is of young adult offspring. Usual dietary intake was assessed using a Food Frequency Questionnaire (FFQ). Data on sociodemographic and lifestyle variables were obtained from self-reports.Results:Western and prudent dietary patterns were identified for the combined cohort of women and men using principal components analysis. Multivariable linear regression models were used to examine the associations between lifestyle variables and dietary patterns adjusting for potential confounders. Results from multivariable adjusted models showed that physical activity, watching TV and smoking were strongly associated with each dietary pattern; alcohol consumption and BMI showed weaker associations (P < 0·05 for all).Conclusions:Our study describes a clustering of unhealthy lifestyles in young adults. Young adults with unhealthy lifestyles less often adhere to a healthy prudent dietary pattern and more often an unhealthy Western pattern. Dietary preferences are enmeshed in a lifestyle matrix which includes physical activity, sedentary activity, smoking and alcohol consumption of young adults.

There is little known about whether exposure to family poverty at specific periods of the early life course independently contributes to coronary heart disease risk beyond the contribution of concurrent poverty. Children were recruited in early pregnancy and additional survey data obtained during the pregnancy and at the 5-, 14- and 30-year follow-ups. Fasting blood samples were also obtained at the 30-year follow-up. Analyses are multinominal logistic regressions stratified by gender and with adjustments for confounding. For male offspring, family poverty at different stages of the early life course was not associated with measures of cardio-metabolic risk. For females early life course, poverty predicted obesity, homeostatic model assessment of insulin resistance (HOMA-IR) and total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C), as well as concurrent family poverty associated with obesity, HOMA-IR, TC/HDL-C, HDL-C and increased systolic and diastolic blood pressure. Family poverty in the early life course independently predicts increased levels of cardio-metabolic risk of females. The primary finding, however, is that concurrent poverty is independently and strongly associated with increased cardio-metabolic risk levels in young adulthood.

Background: Patients with cardiac implantable electronic devices (CIEDs) frequently undergo transthoracic echocardiography (TTE). As a result, incidental mobile echodensities (MEDs) attached to device leads are commonly detected. The aim of this study was to estimate the incidence and clinical outcomes of incidental MEDs on CIED leads. Methods: A retrospective analysis performed between 2011 and 2018 identified 3548 TTE studies performed on 1849 patients with CIEDs. Results: MEDs were identified in 30 patients (1.6%) without clinical suspicion of infective endocarditis (IE). Patients with incidental MEDs were apyrexial, and those tested demonstrated low inflammatory markers and negative blood cultures (BC). In this group, the majority (83%) of MEDs were in the right atrium and no MEDs were detected near the tricuspid valve. Transesophageal echocardiography (TEE) did not influence clinical outcomes. No patient required long-term antibiotics or lead extraction and no IE-related deaths were identified from electronic health records during a mean follow-up period of 43 months (1-89). In contrast, nine patients with suspected IE were all pyrexial with elevated inflammatory markers, had positive BC, and had proven IE. In these cases, the majority of MEDs were at the device lead/tricuspid valve interface. MEDs close to the tricuspid valve were strongly associated with IE (P

Bicuspid aortic valve (BAV) is the most common cardiac congenital abnormality and can be associated with significant valvulopathy or aortopathy. Current active areas of BAV research include prediction of development of valve dysfunction and aortopathy, and the various surgical valvular strategies with or without ascending aortic replacement. There is also increasing interest in the emerging role of transcatheter aortic valve replacement (TAVR) even though it is listed as a relative contraindication in current TAVR recommendations. Although there are clearly established guidelines in the clinical management and surgical techniques for the management of BAV with or without aortopathy, many of these newer surgical techniques have shown excellent post-surgical results but need to be directly compared against “standard” guidelines recommended treatment. As such, this creates new controversies regarding the clinical and surgical management of BAV. In this review, we have summarized the current understan...

Our aim was to determine the feasibility of 18F-florbetaben PET in diagnosing cardiac amyloidosis. Methods: 18F-florbetaben PET was performed on 14 patients: 5 amyloid light chain, 5 amyloid transthyretin, and 4 control with hypertensive heart disease. Qualitative and quantitative assessments of 18F-florbetaben activity were performed using the SUVmean of the left ventricular myocardium and blood pool and calculation of target-to-background SUV ratio. Myocardial 18F-forbetaben retention was also calculated as the percentage mean myocardial SUV change between 0 and 5 min and 15 and 20 min after radiotracer injection. Global left ventricular longitudinal and right ventricular free wall longitudinal strain were calculated using 2-dimensional speckle-tracking echocardiography. Results: Target-to-background SUV ratio and percentage myocardial 18F-forbetaben retention were higher in amyloid patients than in hypertensive controls. A cutoff of 40% was able to differentiate between cardiac amyloid patients and hypertensive controls. Percentage myocardial 18F-forbetaben retention was an independent determinant of both global left ventricular longitudinal and right ventricular free wall longitudinal strain via an inverse curve relationship. Conclusion: 18F-florbetaben PET imaging can accurately identify and differentiate between cardiac amyloidosis and hypertensive heart disease. Percentage myocardial 18F-florbetaben retention was an independent determinant of myocardial dysfunction in cardiac amyloidosis.

This case study describes the development, implementation and review of a sustainable and culturally sensitive procedure for a hospital-funded discharge medicine subsidy for Aboriginal and Torres Strait Islander patients registered with the Closing the Gap (CTG) program discharging from a public hospital. A 7-day fully subsidised medication supply was approved to be offered to Aboriginal and Torres Strait Islander patients admitted under cardiac care teams, including cardiology and cardiothoracic surgery patients. Patients were offered the option of a 7-day supply free of cost to them or a full Pharmaceutical Benefits Scheme (PBS) supply if preferred. A general practitioner (GP) appointment was organised within 7 days of discharge to ensure patients received ongoing supply of their medications as well as timely clinical review after discharge. Over a 34-month period from September 2015 to June 2018, 535 Aboriginal and Torres Strait Islander patients were admitted to the hospital under cardiac care teams. Of these patients, 296 received a subsidised discharge medication supply with a total cost of A$6314.56 to the hospital over the trial period, with a mean cost of A$21.26 per discharge. The provision of subsidised medications through the CTG program has improved the continuity of care for Aboriginal and Torres Strait Islander patients. The culturally sensitive approach is well received and has allowed smooth transition back to the community. This site-specific and state-based funding model was found to be financially sustainable at a public hospital. What is known about the topic?The CTG PBS program is not applicable to discharge prescriptions from public hospitals. As such, patients are required to either leave the hospital with no medicines or leave the hospital with medicines for which they have to pay full PBS price. This creates a huge financial barrier to the care for CTG-registered patients in the acute care setting. What does this paper add?A sustainable solution to the problem was found via a state-funded model while providing a supportive team to ensure GP follow-up and continuity of care after discharge. What are the implications for practitioners?If similar approvals are granted and supported at other public hospital sites, practitioners will be afforded one less barrier to provide patient-centred care for Aboriginal and Torres Strait Islander patients.

Background Current understanding of metabolic heart disease consists of a myriad of different pathophysiological mechanisms. Epicardial adipose tissue (EAT) is increasingly recognized as metabolically active and associated with adverse cardiovascular outcomes. The present study aimed to investigate the effect of increased EAT volume index on left ventricular (LV) myocardial fat content and burden of interstitial myocardial fibrosis and their subsequent effects on LV myocardial contractile function. Methods and Results A total of 40 volunteers (mean age, 35±10 years; 26 males) of varying body mass index (25.0±4.1 kg/m 2 ; range, 19.3–36.3 kg/m 2 ) and without diabetes mellitus or hypertension were prospectively recruited. EAT volume index, LV myocardial fat content, and extracellular volume were quantified by magnetic resonance imaging. LV myocardial contractile function was quantified by speckle tracking echocardiography global longitudinal strain on the same day as magnetic resonance imaging examination. Mean total EAT volume index, LV myocardial fat content, and extracellular volume were 30.0±19.6 cm 3 /m 2 , 5.06%±1.18%, and 27.5%±0.5%, respectively. On multivariable analyses, increased EAT volume index and insulin resistance were independently associated with both increased LV myocardial fat content content and higher burden of interstitial myocardial fibrosis. Furthermore, increased EAT volume index was independently associated with LV global longitudinal strain. Conclusions Increased EAT volume index and insulin resistance were independently associated with increased myocardial fat accumulation and interstitial myocardial fibrosis. Increased EAT volume index was associated with detrimental effects on myocardial contractile function as evidenced by a reduction in LV global longitudinal strain.

Heart failure (HF) and atrial fibrillation (AF) frequently coexist, and they can beget one another due to similar factors and shared pathophysiology. These pathophysiologic changes promote the episodes of AF, while they in turn predispose to the exacerbation of HF. In this review, we will discuss pathophysiological mechanisms shared by AF and HF. Patients with concomitant HF and AF are at a particularly high risk of thromboembolism, which contribute to even worse symptoms and poorer prognosis. Vitamin K antagonists (VKA) (warfarin) were the traditional medication in AF patients for the prevention of stroke, whereas the advance of novel non-VKA oral anticoagulants (NOACs) (dabigatran, apixaban, rivaroxaban, and edoxaban) is challenging these standard prescriptions. NOACs' potential advantages over warfarin, including fixed dosing regimens, wide therapeutic window, and more sustained anticoagulant response, promote clinicians to consider these novel agents in the first place. However, some data suggested patients with AF and HF may receive different therapeutic response than those with AF alone in anticoagulant treatment. Accordingly, we aim to assess the potential role of oral anticoagulants, especially NOACs, in the management of patients with concomitant AF and HF.

Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot. Although EAT volume is associated with the incidence and burden of atrial fibrillation (AF), its role in subclinical left atrial (LA) dysfunction is unclear. This study aims to evaluate the relationships between EAT volumes, LA function, and LA global longitudinal strain.One hundred and thirty people without obstructive coronary artery disease or AF were prospectively recruited into the study in Australia and underwent cardiac computed tomography and echocardiography. EAT volume was quantified from cardiac computed tomography. Echocardiographic 3-dimensional (3D) volumetric measurements and 2D speckle-tracking analysis were performed.Using the overall median body surface area-indexed total EAT volume (EATi), the study cohort was divided into 2 groups of larger and smaller EATi volume. Subjects with larger EATi volume had significantly impaired LA reservoir function (3D LA ejection fraction, 46.1% ± 8.9% vs 49.0% ± 7.0%, P = 0.044) and reduced LA global longitudinal strain (37.6% ± 10.2% vs 44.1% ± 10.7%, P0.001). Total EATi volume was a predictor of impaired 2D LA global longitudinal strain (standardized β = -0.204, P = 0.034), reduced 3D LA ejection fraction (standardized β = -0.208, P = 0.036), and reduced 3D active LA ejection fraction (standardized β = -0.211, P = 0.017). Total EATi volume, rather than LA EATi volume, was the more important predictor of LA dysfunction.Indexed EAT volume is independently associated with subclinical LA dysfunction and impaired global longitudinal strain in people without obstructive coronary artery disease or a history of AF.

Background Although epicardial adipose tissue (EAT) volume is associated with increased incidence of coronary artery disease (CAD), its role in myocardial systolic dysfunction is unclear. The present study aimed to identify independent determinants of EAT volume in patients without obstructive CAD, and to evaluate the association between EAT volume (vs other measures of obesity) and myocardial systolic strain analysis. Methods We prospectively recruited 130 patients without obstructive CAD on contrast-enhanced cardiac computed tomography imaging and normal left ventricular ejection fraction on 3-dimensional (3D) echocardiography. EAT volume was quantified from cardiac computed tomography imaging, and 3D multidirectional (longitudinal, circumferential, radial, and area) strain were measured. Results The mean EAT volume was 97.5 ± 43.7 cm 3 . In multivariable analysis, measures of obesity (body mass index [ P = 0.007] and waist/hip ratio [ P = 0.001]) were independently associated with larger EAT volume. EAT volume was correlated with 3D global longitudinal ( r = 0.601; P r = 0.375; P r = −0.546; P r = 0.558; P P P = 0.006), radial (standardized β = −0.422; P P P > 0.05). Conclusions EAT volume is independently associated with impaired myocardial systolic function despite preserved 3D left ventricular ejection fraction and absence of obstructive CAD, and might play a significant role in the pathophysiology of diabetic, obesity, and metabolic heart disease.

Aortic valve stenosis (AS) is a frequent and potentially severe disease of the heart. Accurate assessment of AS is a critical factor in determining prognosis and treatment. This paper describes the advantages and limitations of AS assessment from a biomechanical engineering perspective, by contrasting the non-invasive AS diagnostic methods of echocardiography (Echo), computed tomography (CT), magnetic resonance imaging (MRI), computational analysis (CA) including the invasive technique of cardiac catheterization. The findings illustrated that current methods of AS evaluation, with assumptions of an ideal fluid, geometry and governing equations may not apply well to the aortic valve pathology and could increase the uncertainty of the degree of stenosis and valve area. This review suggests an alternative method using CA, which could potentially overcome the pitfalls of other AS assessments that incorporate geometry, pressure recovery and aorta wall compliance, based on the accurate conversion of AS imaging to the numerical modelling. Further, this review highlights the importance of CA boundary conditions, and the role of verification and validation to produce reliable computational results.

Background: The CHA2DS2-VASc score is the standard of care in thromboembolic risk assessment for patients with non-valvular atrial fibrillation (AF). Most patients will undergo transthoracic echocardiography (TTE) for further evaluation, and many also having transesophageal echocardiography (TEE) performed prior to cardioversion or ablation. We sought to evaluate the relationship between left atrial (LA) abnormalities detected on TEE and TTE parameters, to determine if imaging may be additive in risk assessment.Methods: Clinical, TEE and TTE data for patients in AF at the time of their study were included in this retrospective analysis. LA/LA appendage (LAA) abnormalities on TEE included the presence of spontaneous echo contrast, sludge, thrombus and LAA emptying velocity 90% in both groups. Median LAVI, septal e’ and E wave velocity in the ≤ 1 vs ≥2 groups were 46ml/m2vs 48ml/m2, 8cm/s vs 6cm/s and 0.8m/s vs 0.8m/s, respectively. Overall, increased LAVI and reduced septal e’ on TTE was associated with TEE LA/LAA abnormalities (p=0.02, p=0.005 respectively). In subgroup analysis, it was found that LAVI and septal e’ was statistically significant in the low CHA2DS2-VASc group (p=0.03, p =0.01), but not in the higher CHA2DS2-VASc group (p=0.21, p=0.30).Conclusion: TEE LA/LAA abnormalities were not infrequently noted in those patients traditionally deemed low risk (CHA2DS2-VASc ≤ 1). LAVI and septal e’ on TTE appear to be associated with LA/LAA abnormalities detected on TEE, which was particularly relevant in lower CHA2DS2-VASc patients and may be additive to conventional clinical risk assessment. Further study is needed to evaluate the role of imaging in AF thromboembolic risk stratification, and whether this translates to prognostic and clinical endpoints.

Coronary vasospasm is an uncommon, but perhaps under-recognised, cause of cardiac arrest. We present a novel case of an exercise-induced out-of-hospital cardiac arrest due to coronary vasospasm, captured on a heartrate monitor, and discuss the management options for this condition.

The renin-angiotensin system is involved in control of blood pressure and salt and fluid homeostasis. Genes for components of this system have been of major focus in research on the causation of the common, complex, polygenic trait, essential hypertension (HT). Association of an A-->C variant at nucleotide 1166 of the angiotensin II type 1 receptor (AT(1)R) gene with HT, but an absence of linkage of this locus with this disease, has been reported recently. Since cofirmation in a different setting is imperative, we performed a cross-sectional case-control study of the Al166C variant in a well-characterized group of 108 Caucasian HT subjects with a strong family history (two affected parents) and early onset disease. Genotyping was by mismatch polymerase chain reaction/BfrI restriction fragment length polymorphism analysis. Frequency of the C-1166 allele was 0.40 in HTs and 0.29 in normotensives. The difference in genotype (chi(2) = 13, P = 0.0015) and allele (chi(2) = 5.3, P = 0.02) frequencies between the two groups was significant (odds ratio for CC vs AA + AC = 7.3 [95% CI, 1.9-31.9). The present results implicate the AT(1)R gene, or a locus in linkage disequilibrium with the variant tested, in the causation of essential HT.

β 2 -Adrenergic receptor gene and neuropeptide Y gene may potentially influence lipid metabolism and overall energy balance. Therefore, we examined associations of these genes with lipid fractions and obesity-related phenotypes in hypertensive subjects. A total of 638 white individuals from 212 Polish families with clustering of essential hypertension were phenotyped for cardiovascular risk determinants. Each subject was genotyped for functional polymorphisms of β 2 -adrenergic receptor gene (Arg16Gly and Gln27Glu) and neuropeptide Y (Leu7Pro). Of 3 common haplotypes of β 2 -adrenergic receptor gene, Arg16Gln27 was overtransmitted to offspring with elevated levels of total cholesterol ( Z =2.2; P =0.026) and LDL-cholesterol ( Z =3.2; P =0.002). Individually, Leu7Pro was not associated with any of the metabolic phenotypes in family-based tests or case-control analyses. However, in the presence of Arg allele of Arg16Gly and Gln allele of Gln27Glu, homozygosity for Leu variant of the Leu7Pro polymorphism was associated with 2.1-increased odds ratio (confidence interval, 1.10 to 3.81; P =0.024) of elevated LDL in hypertensive subjects, independent of age, gender, body mass index, adjusted blood pressures, antihypertensive therapy, and use of nonselective β-blockers and diuretics. Consistently, there was a significant multilocus association among variants of Arg16Gly, Gln27Glu, and Leu7Pro in hypertensive probands with elevated LDL (cases; P =0.028) but not in hypertensive subjects with normal LDL (controls). This study revealed an association of LDL-cholesterol with β 2 -adrenergic receptor gene haplotype and provided evidence for epistatic interaction between β 2 -adrenergic receptor gene and neuropeptide Y gene in determination of LDL-cholesterol in patients with essential hypertension.

To perform association studies of polymorphisms of the potential candidate essential hypertension (HT) genes GRK4, PTP1B and HSD3B1.Subjects consisted of 168 unrelated, Caucasian essential hypertensive (HT) patients and 312 normotensive (NT) controls. Biological power was increased by ensuring subjects in each group had parents with the same blood pressure (BP) status as theirs. Three GRK4gamma variants (R65L, A142V and A486V), one HSD3B1 variant (T---C Leu) and one PTP1B variant (1484insG) were genotyped by polymerase chain reaction and restriction enzyme digestion or by homogenous MassEXTEND Assay.The V allele of the A486V variant of GRK4gamma, but not the R65L or A142V variants, showed an association with HT (P = 0.02). The V allele was also associated with an elevation in systolic blood pressure (SBP) (P = 0.002). Although the L65 and the V142 alleles tracked with elevation in diastolic (DBP), this was seen only in male HTs (P = 0.009; P = 0.002, respectively). Haplotype frequencies differed between the HT and NT groups, particularly for the R, V, V haplotype combination of R65L, A142V and A486V, respectively. Neither of the HSD3B1 or PTP1B variants were associated with HT.Genetic variation in GRK4gamma was associated with HT in the subjects studied.

The CYP11B2 locus is an important candidate region in essential hypertension (HT). We therefore investigated CYP11B2 polymorphisms T-344C, T4986C and A6547G for association with essential HT. This included haplotype analysis and measurement of plasma aldosterone levels.The three single nucleotide polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis of genomic DNA from 146 HT and 291 normotensive (NT) white subjects of Anglo-Celtic descent, in whom parental blood pressure status was the same as the subjects'. Genotype and allele frequencies in HTs and NTs were compared by chi2 analysis. Linkage disequilibrium and haplotype frequencies were estimated by the program 'snphap'. Phenotype-genotype relationships were tested using one-way analysis of variance.The T-344C variant was associated with HT (chi2 = 7.4, P = 0.0064). This association was confined to female HTs (P = 0.0061 for genotypes, P = 0.0013 for alleles). A strong association with HT was also seen for the A6547G variant (P = 0.0015), being greatest in females (P0.0001). No association was seen for the T4986C variant. Haplotype analysis of the three single nucleotide polymorphisms across eight different haplotype combinations showed a significant association with HT (chi2 = 24, seven degrees of freedom, P0.001). No significant tracking of plasma aldosterone with genotype was observed.The T-344C and A6547G, but not the T4986C, variants of the aldosterone synthase gene are associated with HT in females of the Anglo-Celtic population studied. This was reinforced by haplotype analysis.

The gene SAH (chromosome 16p12.3) is of interest in the etiology of human hypertension. In Caucasians a PstI restriction fragment length polymorphism (RFLP) of SAH has been correlated with body weight in individuals with hypertension. To extend this finding we carried out a case-control study of several recently identified polymorphisms in SAH: 1) an insertion/deletion of TTTAA at nucleotide -1037 in the promoter; 2) an insertion/deletion of two Alu like sequences in intron 1; and 3) an A→G variant in intron 12 located 7 bp upstream from exon 13. Subjects were 121 hypertensives with 2 hypertensive parents and 178 normotensives whose parents were both normotensive. All were Anglo-Celtic Caucasians and 51% of the hypertensives were overweight (body mass index (BMI)>25 kg/m2). The SAH promoter and intron 1 variants, but not the intron 12 or PstI RFLP, were in linkage disequilibrium (LD) (D′=100%, p

Background The World Health Organization and the American Diabetes Association recommend a level of glycated hemoglobin (HbA1c) ≥ 6.5% as diagnostic for diabetes. However, concordance between fasting plasma glucose (FPG) and HbA1c levels in acutely unwell patients is unknown. Furthermore, the prognostic value of HbA1c for left ventricular (LV) dysfunction is unclear. This study aimed to evaluate the concordance between HbA1c levels and FPG in consecutive patients with acute ST-elevation MI (STEMI) and compare their prognostic value in predicting LV dysfunction and elevated filling pressures on echocardiography. Methods A total of 142 patients with a first incidence of STEMI were prospectively recruited. LV diastolic function was defined as mean septal and lateral early diastolic velocities (average e'); filling pressure was the ratio of transmitral E velocity to average e' (average E/e'). Results Mean FPG and HbA1c levels were 7.7 ± 2.8 mmol/L and 6.5% ± 1.6%, respectively. Of 109 patients without previous diabetes, HbA1c levels identified an additional 18 patients (16.5%) as having diabetes, and the concordance with FPG was poor. Between diabetic and nondiabetic patients, there were no differences in LV end-diastolic volume (116 ± 37 vs 118 ± 43 mL; P = 0.78), end-systolic volume (69 ± 33 vs 68 ± 35 mL; P = 0.93), and ejection fraction (42 ± 12 vs 44 ± 11%; P = 0.49). On multivariable analyses, average e' was independently associated with HbA1c (β = −0.161; P = 0.045) but not FPG ( P = 0.82). Similarly, average E/e' was independently associated with HbA1c (β = 0.168; P = 0.04) but not FPG ( P = 0.32). Receiver operating characteristic curve analysis showed that an HbA1c cutoff of 6.4% (area under the curve, 0.68; P = 0.002) was associated with an elevated LV filling pressure. Conclusions Only HbA1c was independently associated with impaired LV diastolic function and increased filling pressures after STEMI.

BACKGROUND The presence of entrapped lung changes the appropriate management of malignant pleural effusion from pleurodesis to insertion of an indwelling pleural catheter. No methods currently exist to identify entrapped lung prior to effusion drainage. Our objectives were to develop a method to identify entrapped lung using tissue movement and deformation (strain) analysis with ultrasonography and compare it to the existing technique of pleural elastance (PEL). METHODS Prior to drainage, 81 patients with suspected malignant pleural effusion underwent thoracic ultrasound using an echocardiogram machine. Images of the atelectatic lower lobe were acquired during breath hold, allowing motion and strain related to the cardiac impulse to be analyzed using motion mode (M mode) and speckle-tracking imaging, respectively. PEL was measured during effusion drainage. The gold-standard diagnosis of entrapped lung was the consensus opinion of two interventional pulmonologists according to postdrainage imaging. Participants were randomly divided into development and validation sets. RESULTS Both total movement and strain were significantly reduced in entrapped lung. Using data from the development set, the area under the receiver-operating curves for the diagnosis of entrapped lung was 0.86 (speckle tracking), 0.79 (M mode), and 0.69 (PEL). Using respective cutoffs of 6%, 1 mm, and 19 cm H 2 O on the validation set, the sensitivity/specificity was 71%/85% (speckle tracking), 50%/85% (M mode), and 40%/100% (PEL). CONCLUSIONS This novel ultrasound technique can identify entrapped lung prior to effusion drainage, which could allow appropriate choice of definitive management (pleurodesis vs indwelling catheter), reducing the number of interventions required to treat malignant pleural effusion.

Tumor necrosis factor (TNF) receptor 2 (TNF-R2) has been implicated in insulin resistance and metabolic syndrome disorders, one of which is hypertension (HT). We therefore decided to test markers in and near the TNF-R2 gene ( TNFRSF1B) for linkage and association with HT, as well as hypercholesterolemia, and plasma levels of the shed soluble receptor (sTNF-R2). The linkage study, which involved 200 HT Anglo-Celtic Caucasian sibpairs, indicated a sharp, significant linkage peak centered at TNFRSF1B (multipoint maximum LOD score = 2.6 and 3.1 by weighted and unweighted MAPMAKER/SIBS, respectively; two-point LOD scores = 2.9 and 3.9 by weighted and unweighted SPLINK, respectively; P = 10 –4 by identical-by-state χ 2 ). The case–control study in 134 unrelated HTs who were the offspring of two HT parents and 197 normotensives (NTs) whose parents were both NTs, indicated possible association of TNFRSF1B with HT by haplotype analysis (P = 0.008). Plasma sTNF-R2 was elevated in HTs (P < 0.0001) and showed a correlation with systolic and diastolic blood pressure (BP )( P

A Gly460Trp variant of the cytoskeletal protein alpha-adducin has recently been implicated in the etiology of essential hypertension (HT) in a study involving southern European whites. We attempted to replicate this finding in a well-characterized, extensively studied group of 112 white Australians with essential HT, with strong family history (two HT parents), early-onset, moderate to severe disease, and of British extraction. Controls were 196 normotensive (NT) white subjects whose parents were both NT older than age 50 years. A mismatch polymerase chain reaction method involving BanII was developed for genotyping. Frequency of the Trp460 allele was 0.23 in the HT and 0.24 in the NT groups (chi2 = 0.2, P = .7). No association was observed with blood pressure, body mass index, age, plasma renin, angiotensinogen, angiotensin converting enzyme, cholesterol, triglycerides, or HDL or LDL cholesterol. Our results therefore provide no support for a role for the alpha-adducin variant in hypertension, at least in our severely affected Anglo-white group with strong family history of HT.

Recurrent pulmonary embolism (PE) in prothrombotic patients with patent foramen ovale (PFO) is not considered a setting for elective PFO closure. We describe a 35-year-old woman with known PFO, recurrent PE on warfarin, and Klippel-Trenaunay syndrome-a condition with predisposition for thromboembolism-who suffered concurrent saddle PE and devastating stroke with further impending paradoxical embolus across the PFO. Optimal management in patients with biatrial thromboembolus caught in transit across PFO is challenging. Patients with recurrent PE, prothrombotic states, and PFO should be considered for PFO closure. Prompt diagnosis of impending paradoxical embolus with echocardiography and consideration of surgical removal and PFO closure are critical.

OBJECTIVE: Only a small fraction of coronary artery disease (CAD) heritability has been explained by common variants identified to date. Interactions between genes of importance to cardiovascular regulation may account for some of the missing heritability of CAD. This study aimed to investigate the role of gene-gene interactions in common variants in candidate cardiovascular genes in CAD. APPROACH AND RESULTS: 2,101 patients with CAD from the British Heart Foundation Family Heart Study and 2,426 CAD-free controls were included in the discovery cohort. All subjects were genotyped with the Illumina HumanCVD BeadChip enriched for genes and pathways relevant to the cardiovascular system and disease. The primary analysis in the discovery cohort examined pairwise interactions among 913 common (minor allele frequency >0.1) independent single nucleotide polymorphisms (SNPs) with at least nominal association with CAD in single locus analysis. A secondary exploratory interaction analysis was performed among all 11,332 independent common SNPs surviving quality control criteria. Replication analyses were conducted in 2,967 patients and 3,075 controls from the Myocardial Infarction Genetics Consortium. None of the interactions amongst 913 SNPs analysed in the primary analysis was statistically significant after correction for multiple testing (required P 1.7 for common variants in the primary analysis. CONCLUSIONS: Moderately large additive interactions between common SNPs in genes relevant to cardiovascular disease do not appear to play a major role in genetic predisposition to CAD. The role of genetic interactions amongst less common SNPs and with medium and small magnitude effects remain to be investigated The Wellcome Trust Case-ControlConsortium 2 was funded by the Wellcome Trustunder award 085475. The Myocardial InfarctionGenetics Consortium (MIGen) was funded by grantR01 HL087676 from the National Institutes of Health,USA. The replication analysis was funded by grantsfrom the Fondo de Investigación Sanitaria-InstitutoCarlos III/European Development Research Funds(Red de Investigación Cardiovascular RD12/0042/0013, RD12/0042/0061), Fundació Marato TV3(1081810). GL was funded by the Juan de la CiervaProgram, Ministerio de Educación (JCI-2009-04684)

Chromosome 1p36 has been linked to essential hypertension and systolic blood pressure. This locus contains the chloride channel-Kb gene (CLCNKB) and the tumour necrosis factor receptor 2 gene (TNFRSF1B). Polymorphisms of each of these have shown association with hypertension, and a CLCNKB T481S variant alters receptor function. Here we performed association studies in a well-characterized cohort of hypertensives and normotensives whose blood pressure status matched that of both their parents.The study involved 196 essential hypertensives and 321 normotensives. These were genotyped for TNFRSF1B variants T-1710A upstream, A257G in exon 2, a CA-repeat polymorphism in intron 4, E232K and M196R in exon 6, and T1668G and T1690C in the 3'-untranslated region, and the T481S variant of CLCNKB.The CLCNKB T481S variant showed no association with hypertension. Thermodynamic modelling of the 3'-untranslated region of TNFRSF1B mRNA predicted that the T1668G variant alters the stem-loop structure and thus the mRNA stability and expression. However, neither this nor the other TNFRSF1B polymorphisms, either alone or after haplotype analysis, were associated with hypertension. Moreover, for each gene the blood pressure, body mass index, plasma sodium and plasma lipid concentrations were generally similar across genotypes.Our data fail to support previous association findings for TNFRSF1B and CLCNKB at the chromosome 1p36 locus implicated in hypertension.

Several lines of evidence suggest the involvement of the human endogenous retrovirus (HERV)-K18 in the etiology of type 1 diabetes. HERV-K18 encodes for a T-cell superantigen (SAg). T-cells with T-cell receptor Vβ7 chains reactive to the SAg and HERV-K18 mRNA were enriched in the tissues at the onset of the disease. HERV-K18 transcription and SAg function in cells capable of efficient presentation are induced by proinflammatory stimuli such as viruses and interferon-α and may trigger progression of disease to insulitis or from insulitis to overt diabetes. Allelic variation of HERV-K18 or the DNA flanking it, the CD48 gene, could modulate genetic susceptibility. Analysis of 14 polymorphisms in the locus using 754 diabetic families provided positive evidence of association of three variants belonging to a single haplotype (P = 0.0026), present at 21.8% frequency in the population. Genotype analysis suggested a dominantly protective effect of this haplotype (P = 0.0061). Further genetic and functional analyses are required to confirm these findings.

A region on human chromosome 5 (5q31.1-qter) contains several genes that encode important blood pressure regulators and thus is a good candidate for analysis of linkage and association with hypertension. We recruited 638 individuals from 212 Polish pedigrees with clustering of essential hypertension. These subjects were genotyped for 11 microsatellite markers that span this region to test for linkage to essential hypertension and systolic and diastolic blood pressures. The segment of this region of ≈7 cM delineated by D5S1480 and D5S500 markers was linked to blood pressures in multipoint analysis. In 2-point analysis, D5S1480—the marker in close proximity to β 2 -adrenergic receptor gene—reached the maximal linkage to essential hypertension and adjusted systolic and diastolic blood pressures, implicating this gene as a positional candidate for further association studies. Arg16Gly, Gln27Glu, and Thr164Ile—3 functional single nucleotide polymorphisms within the β 2 -adrenergic receptor gene—were tested for association with essential hypertension. None of these polymorphisms showed a significant association with essential hypertension, separately or in the haplotype analysis. This study provided evidence of linkage of 5q31.1-5qter region to essential hypertension in the European population. Moreover, it implicated the chromosomal segment in close proximity to D5S1480 and D5S500. The detailed analysis of 3 single nucleotide polymorphisms does not support the role of the β 2 -adrenergic receptor gene as a major causative gene for the detected linkage.

Background — Elevated pulse pressure is associated strongly with adverse cardiovascular outcome; however, the genetic basis of this condition is unknown. This study examined whether genotypic variation in the extracellular matrix protein fibrillin-1, the Marfan gene, was associated with aortic stiffening and therefore could contribute to cardiovascular risk associated with pulse pressure elevation in coronary disease. Methods and Results — Patients (n=145; 113 men), 62±9 years of age (mean±SD), with angiographically confirmed coronary disease, were studied. Carotid applanation tonometry was used to assess central blood pressures, and in conjunction with Doppler velocimetry, to assess aortic input and characteristic impedance. Fibrillin-1 genotype was characterized by a variable nucleotide tandem repeat and 2 single-nucleotide polymorphisms. The variable nucleotide tandem repeat was a good predictor of underlying haplotypes with 3 genotypes (2-2, 2-4, and 2-3) accounting for 86% of the population. The 2-3 genotype had higher input impedance ( P =0.002), characteristic impedance ( P =0.005), and carotid pulse pressure ( P =0.002) compared with the 2-2 and 2-4 genotypes. Disease severity assessed by previous angioplasties and the number of patients with a stenosis >90% was also greater in the 2-3 genotype. Furthermore, in a multivariate analysis, fibrillin-1 genotype and central pulse pressure were independent of conventional risk factors in determining coronary disease severity. There was no difference in age, sex ratio, body mass index, smoking status, cholesterol level, or medication among the 3 genotypes. Conclusions — Although a causative link has not been shown, these data are consistent with an important role for fibrillin-1 genotype in cardiovascular risk associated with large-artery stiffening and pulse pressure elevation in individuals with coronary disease.

Introduction: Risk assessments for predicting post-operative complications after cardiac surgery are rarely studied compared to mortality. Objectives: We compared EuroSCORE, EuroSCORE II, and Society of Thoracic Surgeon’s (STS) Score and an Australasian model (Aus-AVR Score) for predicting morbidities after aortic valve replacement (AVR), and also evaluated seven STS complications models in this context. Methods: We retrospectively calculated all risk scores for the 620 patients undergoing isolated AVR at Auckland City Hospital during 2005-2012, and assessed their discrimination and calibration for post-operative complications. Results: Amongst the mortality scores, EuroSCORE was the best at discriminating stroke (c-statistic 0.845); EuroSCORE II at deep sternal wound infection (c1⁄40.748); and STS Score at composite morbidity or mortality (c1⁄40.666), renal failure (c1⁄40.634), ventilation >24 hours (c1⁄40.732), return to theatre (c1⁄40.577) and prolonged hospital stay >14 days post-operatively (c1⁄40.707). The individual STS complications models had slightly higher c-statistic (c1⁄40.634-0.846) for all complications except deep sternal wound infection, and had good calibration (Hosmer-Lemeshow test P-value 0.123-0.915) for all complications, including when divided in quintiles. Independent predictors for composite morbidity outcomes were age, critical pre-operative state, urgent surgery and dialysis. Conclusion: The STS Score was overall the best at discriminating post-operative complications and their composite for AVR. All STS complications model except for deep sternal wound infection had good discrimination and calibration for post-operative complications. Operation and complications specific models improve the detection of these outcomes in AVR. Disclosure of Interest: None Declared

Background Blood pressure is a determinant of the risk of stroke among both hypertensive and non-hypertensive individuals with cerebrovascular disease. However, there is uncertainty about the efficacy and safety of blood-pressure-lowering treatments for many such patients. The perindopril protection against recurrent stroke study (PROGRESS) was designed to determine the effects of a blood-pressure-lowering regimen in hypertensive and non-hypertensive patients with a history of stroke or transient ischaemic attack. Methods 6105 individuals from 172 centres in Asia, Australasia, and Europe were randomly assigned active treatment (n=3051) or placebo (n=3054). Active treatment comprised a flexible regimen based on the angiotensin-converting-enzyme inhibitor perindopril (4 mg daily), with the addition of the diuretic indapamide at the discretion of treating physicians. The primary outcome was total stroke (fatal or non-fatal). Analysis was by intention to treat. Findings Over 4 years of follow up, active treatment reduced blood pressure by 9/4 mm Hg. 307 (10%) individuals assigned active treatment suffered a stroke, compared with 420 (14%) assigned placebo (relative risk reduction 28% [95% Cl 17-38], p

Abstract —Suggestive evidence has been obtained in a “4-corners” study for involvement of the glucocorticoid receptor gene ( GRL ) in genetic variation in blood pressure. Therefore, we tested markers at the GRL locus for association and linkage with essential hypertension (HT). For the association study, we used a well-characterized group of 129 white Australians of Anglo-Celtic extraction who had HT, a strong family history of HT (2 parents with the disease), and early-onset moderate-to-severe disease. Controls were 195 normotensive white subjects whose parents were normotensive past the age of 50 years. For the linkage study, we used 175 sibling pairs of similar ancestry. The case-control groups were genotyped for an Asn363Ser variant in exon 2, a G/T variant in intron 4, and a microsatellite marker ( D5S207 ) tightly linked (GRL . For the groups as a whole, no association or linkage was observed after analysis of data by a variety of statistical tests. Analysis of sibling-pair data gave an exclusion score of −3.8 for the logarithm of the odds for linkage, indicating significant nonlinkage. However, in females, weak association of the intron 4 polymorphism with HT ( P =0.03), as well as with systolic and diastolic blood pressure in all subjects ( P =0.04 and 0.03), was observed, and in the case of the D5S207 marker, association with HT was apparent in males ( P =0.0001). Thus, although our results provide no overall support for GRL in HT etiology, apparent gender-specific associations could exist in this genomic region, possibly reflecting correlated occurrence with (an)other metabolic syndrome disorder(s).

Abstract —A locus for essential hypertension has been found recently on chromosome 17 in the general vicinity of the inducible nitric oxide synthase (iNOS) gene ( NOS2A at 17cen-q11.2). We therefore tested NOS2A markers for association and linkage with hypertension in affected Australian Anglo-Caucasians. Patients for the association study (n=112) were from our cohort of hypertensives (systolic/diastolic=175±25 SD/112±19 mm Hg) who were the offspring of 2 hypertensive parents; control subjects (n=164) were normotensives whose parents were both normotensive. The linkage study involved 156 hypertensive sib-pairs. Genotypes for an 8-allele pentameric repeat located 2.6 kb upstream of NOS2A and of a biallelic tetranucleotide repeat 0.7 kb upstream were determined by polymerase chain reaction and automated gene scan analysis. In the association study, the frequency of the minor allele of the biallelic marker was 0.18 in the hypertensives and 0.14 in the normotensives (χ 2 1 df =1.1, P =0.3). Allele frequencies for the multiallelic marker were also similar in each group (χ 2 7 df =9.8, P =0.2). Furthermore, no genotypic differences in blood pressure were apparent. In the sib-pair study, SPLINK APM, and MAPMAKERS/SIBS did not indicate excess allele sharing. We also examined genotype as a function of age. In the younger (< 60 years) hypertensives as well as younger or older normotensives, genotype and allele frequency of the biallelic marker was similar (0.12 to 0.14). However, in hypertensives ≥60 years of age, frequency of the minor allele was 0.28 (χ 2 =7.4, P =0.006). Homozygotes for this allele were rare. Frequency of heterozygotes was 0.19 for normotensives but 0.39 for the older hypertensives (χ 2 =8.0, P =0.018) and was 0.40 for hypertensive sibs ≥60 years of age with a diastolic pressure ≥100 mm Hg. Furthermore, homozygotes for the major allele were 7 years younger than heterozygotes ( P =0.05 by ANOVA). In conclusion, the present study shows (1) no evidence for a role of NOS2A in hypertension and (2) a genotypic difference in frequency of a NOS2A promoter variant in older hypertensives, seen in 2 different cohorts. A possible interpretation of the latter observation is that NOS2A genotype could affect longevity, at least in patients at high risk by having moderate to severe hypertension.

reoperative cardiac surgery: frequency, characterization, and rescue. J Thorac Cardiovasc Surg 2008;135:316–23, e316. [2] Khan N, Yonan N. Does preoperative computed tomography reduce the risks associatedwith re-do cardiac surgery? Interac CardioVasc Thorac Surg 2009;9:119–23. http://dx.doi.org/10.1016/j.hlc.2013.03.019 Monday 12 November – Session 2/1700 – 1710 Severe Aortic Regurgitation, Aortic Valve Preserving Procedures: A Viable Alternative to Prosthetic AVR Pallav Shah1, Sudhir Wahi 2, Arnold Ng2, William Wang2, Terri hall 2, Alasdair Watson1,∗, Paul Peters 1 1Department of Cardiothoracic, Princess Alexandra Hospital, Brisbane, Australia 2 Department of Cardiology, Princess Alexandra Hospital, Brisbane, Australia Introduction:This studywas undertaken to examine the clinical and echocardiographic outcomes following aortic valve preserving procedures (AVPP: Valve sparing root and Primary valve repair). Methods: Forty-six patients were operated during the study period September 2008 to September 2012. Valve sparing root: 25/46 (54%) patients [Grade of AR: Trivial to mild – 15/25 (60%); Type: Reimplantation-24, Remodelling-1; Valve: Tricuspid-24, Bicuspid-1; Aetiology: Rootdilation (Ib, 2marfans)-20,TypeAdissection5]. 13/25 (52%) had associated cusp prolapse repair. Primary repair: 21/46 (46%) patients [Grade of AR: Severe-16/21 (76%); Valve: Tricuspid-6 (Type Ic-2, Type II4), Quadricuspid-1(Type II), Bicuspid type 1 (with raphe)-7 (Type Ic: 1, TypeII-5, Type III-1), Type A dissection: 7]. Associated elective procedures were CABG: 9 and Hemiarch: 6. Preoperative investigations included 2D and 3D TTE, TOE and Cardiac CT in all patients. Cardiac CT scan proved more accurate in annular and sinus diameters as compared to TOE. (El Khoury classification*; Type I: normal cusp motion [Ia: ascending aortic aneurysm, Ib: aortic root aneurysm, Ic: annular dilation]; Type II: cusp prolapse; Type III: restrictive cusp motion). Results: Thirty-day-mortality: 1/46 (2.2%, redo aortic dissection); Late mortality: 1/45 (2.2%, saddle PE); 30 day morbidity: Reexploration for bleeding-1(2.2%), pacemaker 3 (7%), no strokes. Mean follow-up of 22 months (range: 1–44 months). Clinical and echocardiographic review were done at six weeks, six-monthly for the first year and yearly thereafter. 38/45(85%) were in NYHA class 1. All on aspirin, none received anticoagulation, no incidence of ACH or I.E. One patient had right sided haemianopia (in AF preop). Valve function: Aortic regurgitation (AR) Valve sparing root: 22/24 (92%) had none to mild non progressive centralAR.Onepatient (bicuspid), developed severeAR three months post operative and required reoperation. Primary repair: 17/21 (81%) had trace to mild non progressive central AR.1/21 (tricuspid) has eccentric mild AR. 2/21(10%, 1-bicuspid, 1-tricuspid) has progressive central AR from none to mild at three year follow-up. 1/21 patient (bicuspid, type III restrictive) had no AR (severe preop) but has moderate aortic stenosis. Gradients: Valve sparing root; mean gradients: 2–8mm. Primary repair; mean gradients: 8–15mm. Type A Aortic dissection: 12/45 (27%).8/12 had severe preop AR. 5: valve sparing reimplantation and 7: (refashioning of STJ + cusp prolapse repair + subcommurissral annuloplasty). One mortality in redo aortic dissection. No reexploration for bleeding or stroke. All on aspirin, with trace to mild central non progressive AR in 10/11 (90%) patients at latest follow up. Conclusion:AVPP can be performed safely with acceptable outcomes. Long-term clinical and echocardiographic follow-up is essential. http://dx.doi.org/10.1016/j.hlc.2013.03.020 Monday 12 November – Session 2/1710 – 1720 Early Experience of Surgical TAVI – Approaches and Results Paul Wiemers ∗, May Tsai, Karl Poon, Darren Walters, Peter Tesar, Andrew Clarke The Prince Charles Hospital, Chermside, Australia Introduction: Transcatheter aortic valve implantation (TAVI) is nowawell recognisedprocedure for the high risk surgical patient with native or bioprosthetic aortic valve stenosis. Transfemoral and transapical implantation techniques are well described. We describe our early surgical TAVI experience including our adoption of a transaortic implantation technique due to its potential advantages. Methods: We retrospectively reviewed a systemised database and patient records for all patients undergoing surgical TAVI from the commencement date in our centre in 2/2010 to current. Results: A total of 45 patients with a mean age of 81.02± 5.65 yrs have undergone surgical TAVI in our centre. Twenty-nine of these procedures were performed transapically while the most recent 16 procedures were performed via a transaortic route. A significantly higher NYHAclassification (3.13 vs. 2.79; p= 0.036) and lower preprocedural LVEF (55.8 vs. 63.6%; p= 0.021) was observed in the transaortic group. The transapical group trended towards a higher predicted operative mortality (25.35 vs 18.59%; p= 0.082). Significant improvements were predictably observed in mean pressure gradients (MPG) across the aortic valve (47.8–13.0mmHg; p=

D. Harrop1,∗, M. Fryer 1, V. Indrajith 1, S. Butterly 2, B. Lowe3, A. Ng1,4, W. Wang1,4 1 Department of Cardiology, Princess Alexandra Hospital, Brisbane, Australia 2 Department ofCardiovascularMedicine, Sir CharlesGairdner Hospital, Perth, Australia 3 Department of EmergencyMedicine, Princess Alexandra Hospital, Brisbane, Australia 4 University of Queensland, School of Medicine, Brisbane, Australia

The evidence base for echocardiography in blunt chest trauma remains an area of ongoing investigation. Based on first principles, contemporary real world practicemandates echocardiography testing in patients with cardiac specific biomarker (troponin (TnI)) elevation. Prediction of echocardiogram abnormalities based on TnI elevation has not been formally evaluated in this patient category. Methods: Retrospective analysis of all patients presenting with blunt chest trauma, without established underlying cardiac disease, over a calendar year, included in a trauma database in our tertiary hospital. All patient presentations with chest trauma were reviewed and TnI values and echocardiograms independently audited. Results: 337 patients presented to our tertiary trauma centre secondary to blunt force chest trauma during a full 631

Conclusion: ApHCM is a rare condition and colour Doppler and CE imaging can be helpful in its diagnosis by improving the visualisation of ventricular morphology with the incremental benefit of visualising CALVF. The selected use of CE for equivocal cases of ApHCM can improve diagnosis by TTE. doi:10.1016/j.hlc.2011.05.479